![]() ![]() Since many hypotheses concerning the pathogenesis of asthma have been developed from animal models, it is necessary to determine the relevance of these animal models with respect to human tissues. Hence, in order to investigate a potential role for ASM in asthma, it is first necessary to characterise the mechanical properties of nonasthmatic ASM. Much of our current knowledge about ASM contractile function has come from studies in other mammalian species, which may not adequately represent human tissue. One major hurdle in determining whether ASM is truly dysfunctional in asthma is the lack of adequate data on the mechanical properties of human ASM. Although it is generally agreed that the narrowing is caused by ASM shortening, it is still unclear if the excessive narrowing is due to fundamental changes in the phenotype of the smooth muscle itself, or if it is caused by structural and/or mechanical changes in the noncontractile elements of the airway wall, or by alterations in the relationship of the airway wall to the surrounding lung parenchyma 4. Asthma is characterised by episodes of increased airway resistance due to exaggerated airway narrowing. While the physiological function of airway smooth muscle (ASM) is unclear 1– 3, its contraction and subsequent shortening act to increase airway resistance in the lung. These results suggest that human ASM shares similar contractile mechanisms with other animal species and provides an important dataset for comparisons with animal models of disease and asthmatic ASM. Force generation, shortening capacity and velocity were all similar to other mammalian ASM. It is capable of undergoing length adaptation and responds to mechanical perturbation like ASM from other species. Healthy human ASM was found to be mechanically and ultrastructurally similar to that of other species. The ultrastructure of the cells was also examined. The mechanical properties measured included: maximal stress generation, force–length properties, the ability of the muscle to undergo length adaptation, the ability of the muscle to recover from an oscillatory strain, shortening velocity and maximal shortening. In the current study, we sought to define the mechanical properties of healthy human ASM using tissue from intact lungs and compare these properties to measurements in other species. Limited data on human ASM mechanics prevents proper comparisons between healthy and asthmatic tissues, as well as human and animal tissues. ![]() Much of our current understanding about ASM mechanics comes from measurements made in other species. However, whether asthmatic ASM is mechanically different from nonasthmatic ASM is unclear. Airway smooth muscle (ASM) plays a vital role in the exaggerated airway narrowing seen in asthma. ![]()
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